Hematology Problems

What 3 ways can a body have anemiaDecreased production of RBC's; Blood Loss; Increased RBC destruction
Anemia r/t decreased production of RBC'sDecreased hemoglobin synthesis - bone marrow is not producing enough Defective DNA synthesis - congenital (ex: Sicle cell & thalesemia)
Anemia r/t blood lossAcute (ex: car wreck) Chronic (ex: GI Bleeds in elderly; menstruating women)
Anemia r/t increased RBC destruction(the body destroys) Intrinsic - congenital (ex: sicle cell - genetic) Extrinsic - chemotherapy - meds - radiation



Physiologic Effects of AnemiaResult from tissue hypoxia and compensatory mech - (^HR); Dec O2-casrrying capacity of blood; Hgb give up O2 easier to tissues; Blood goes to vital organs first; Inc cardiac output ^HR, ^BP; Inc rate of RBC production
Hbg Level of Mild Anemia10-14
S/S of mild anemiaPalpitations, dyspnes, diaphoresis
Hgb Level of Moderate Anemia6-10
S/S of Moderate AnemiaInc. Cardiopulmonary s/s - chest pain; Pallor, Jaundice, Pruritis, Changes in fingernails - spoon-shaped, pale nail beds
Cardiopulmonary changes r/t anemiaTachycardia, Tachypnea, dyspnea
Cardiopulmonary changes r/t anemia with prolonged chronic anemiaMurmurs, bruit in carotid, Angina, MI, CHF
Neurologic Changes r/t anemiaHA because of lack of O2, Vertigo, Mood changes, Impaired through process
GI Changes r/t anemiaAnorexia, Hepatomegaly, Splenomegaly
Musculosketal Changes r/t anemiaBone pain because bone marrow is stimulated and is making more RBC
General s/s of anemiaFatigue, weight loss, lethargy, sensitivity to cold
Etiology of Iron Deficiency AnemiaInadequate dietary intake Malabsorption Blood loss & not replacing it; Over time - GI bleed Hemolysis - breaking down cells too quickly
Nutrients needed for erythropoiesisIron, Vitamin B 12 - cobalamin, Folic Acid, Proteins, Enzymes, Minerals - Fe & Calcium
Nursing Implications of Iron PrepsAbsorbed best in acidic environment, Cause GI Upset, Liq preps stain teeth, Constipation, Black, Tarry stools; IV preferred(irritating) but can be given Z-track)
Most important nursing diagnosis r/t anemiaRisk for Injury!!
Thalassemiapatient's make defective protein; cells are being broken down (^jaundice); Mediterranean ethnic groups
Thalassemia MinorRecessive trait - little bit
Thalassemia MajorPoor Prognosis
Aplastic AnemiaRare stem cell disorder; do not produce WBC, RBC or Platelets; Can be congenital or acquired
S/S of Aplastic AnemiaS/S of anemia, Bleeding, Infection
Etiology of Acquired Aplastic AnemiaRadiation, Chemicals, Drugs, Chemo drugs, Infection, Pregnancy, Idiopathic
Dx of Aplastic AnemiaA bone marrow that is called a "dry tap"
Tx of Aplastic AnemiaBone marrow transplantation/ immunosuppressant drugs
Anemia Caused by Blood loss can be bothacute & chronic
Acute blood loss r/t anemia can causeHypovolemic shock (see dramatic symptoms); decreased O2 carrying capacity (ex: car accident)
Anemia caused by chronic blood lossdepletion of iron stores - body compensates (ex: GI bleed, heavy periods)
Def of Hemolytic Anemiaanemia caused by increased erythrocyte destruction
Etiology of Hemolytic Anemia(NOT Fe Deficiency) Premature destruction of RBC Increased hematopoeisis Increased reticulocytes Normochromic, normocytic RBC's
Causes of Hemolytic Anemia can beintrinsic and extrinsic
Causes of Intrinsic Hemolytic AnemiaRBC membrane defects, Hgb structure defect, Inherited enzyme defects
Causes of Extrinsic Hemolytic AnemiaDrugs, chemicals, toxins, trauma, burns
Definition of Sickle Cell AnemiaHomozygous recessive heredity - have to have 2 parents carry trait; African American
Pathophysiology of Sickle Cell AnemiaDecreased O2 tension, have abnormal Hgb, RBC's enlongated and obstruct capillaries - get stuck - occludes circulation; Ischemia and infarction
Manifestations of Sickle CellClassic s/s of anemia, Damage to organs - heart, lungs, kidneys, Priapism, Hand-foot syndrome, Susceptible to infection
Priapismpenile erection that won't go away - painful
Dactylitiseffect on hands/feet - malformed
Manifestations of Sickle Cell in ChildrenSmall, short, thin, Delayed growth & development, Acute splenic sequestration, Dactylitis
Acute splenic sequestrationBlood gets trapped in spleen - spleen enlarges - goes into shock and can die in 30 minutes (under age 2)
Sickle Cell patient's can developblindness, Stroke, chest/abd pain, painful joints, freq. pneumonia, enlarged hearet, fever
Triggers of a Sickle Cell CrisisHypoxia, Dehydration, Infection, Overexertion, Anesthesia, Weather changes, Alcohol, Smoking
Tx of Sickle Cell CrisisHOP - Hydration, Oxygenation, Pain Relief
Manifestations of a Sickle Cell CrisisINTENSE PAIN, fever, Tissue hypoxia - - tissue pain & death
Dx of Sickle Cell AnemiaPeripheral smeal, Sickle cell preparation, Hemoglobin electrophoresis
Care for Patient with Sickle Cell AnemiaRest, Analgesia, Oxygen, Hydration, Treat precipating factors, Hydroxyures, Transfusion tx if Hgb dec., Therapeutic apheresis
General management of Sickle Cell AnemiaVaccination against everything, Hydration, Trigger avoidance, Prophylactic antibiotics, Bone marrow transplant, Client education, Good nutrition
Polycythemia meansmany cells - affects all cells
Patho of PolycythemiaMyeloproliferative disorder - bone marrow; Increased production of cells, Increased blood viscosity & volume, Congestion of organs/tissue; splenomegaly
S/S of Polycythemia VeraHypertension, HA, Tinnitus, Blurred vision, Cyanosis, Plethora, Fatigue, Pruritus, Pain in extremities, Night sweats, Wt. Loss, Epistaxis, GI bleeding, Dizziness
Complications of PolycythemiaCHF, CVA, Thrombophlebitis, Hemorrhage, Hyperuricemia
Dx tests for Polycythemia^ H/H, ^WBC, basophilia, ^platelets & platelet dysfunction, ^alkaline phos, uric acid, cobalamin, ^ histamine
Care for a patient with PolycythemiaPhlebotomy - bleed them, Hydration, Bone marrow suppressant drugs, anti-immune drugs, Allopurinol, anti-platelets
Nursing care for a patient with PolycythemiaControl of COPD, Phlebotomy, Fluid management, safe medication mgmt, Prevention of thrombus formation
Primary Polycythemia affectsall cells
Secondary Polycythemia affectsRBC's only - NO itching, NO bleeding, Elevated Hct
Secondary Polycythemia occurs fromCOPD because the lack of O2 causes increaased RBC production

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